| Transient ischemic attack | |
|---|---|
| Classification and external resources | |
| ICD-10 | G45.9 |
| ICD-9 | 435.9 |
| DiseasesDB | 13253 |
| MedlinePlus | 000730 |
| eMedicine | emerg/604 |
| MeSH | D002546 |
A transient ischemic attack (spelled ischaemic in British English)[1] (abbreviated as TIA, often referred to as mini stroke) is a transient episode of neurologic dysfunction caused by ischemia (loss of blood flow) – either focal brain, spinal cord or retinal – without acute infarction (tissue death). TIAs share the same underlying etiology (cause) as strokes: a disruption of cerebral blood flow (CBF). TIAs and strokes cause the same symptoms, such as contralateral paralysis (opposite side of body from affected brain hemisphere) or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech and mental confusion. But unlike a stroke, the symptoms of a TIA can resolve within a few minutes or 24 hours. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke or a silent stroke.[2][3] A silent stroke or silent cerebral infarct (SCI) differs from a TIA in that there are no immediately observable symptoms. A SCI may still cause long lasting neurological dysfunction affecting such areas as mood, personality and cognition. A SCI often occurs before or after a TIA or major stroke.[4]
A cerebral infarct that lasts longer than 24 hours but fewer than 72 hours is called a reversible ischemic neurologic deficit or RIND.
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Symptoms vary widely from person to person, depending on the area of the brain involved. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax); difficulty speaking (aphasia); weakness on one side of the body (hemiparesis); and numbness or tingling (paresthesia), usually on one side of the body. Impairment of consciousness is very uncommon. There have been cases of temporary and partial paralysis affecting the face and tongue of the afflicted. The symptoms of a TIA are short-lived and usually last a few seconds to a few minutes and most symptoms disappear within 60 minutes. Some individuals may have a lingering feeling that something odd happened to the body. Dizziness, lack of coordination or poor balance are also symptoms related to TIA. Symptoms vary in severity.
The most common cause of a TIA is an embolus that occludes an artery in the brain. This usually arises from a dislodged atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart because of atrial fibrillation. In a TIA, the blockage period is very short-lived and hence there is no permanent damage.[5] The cholesterol build-up is gradual and eventually narrows the lumen. With time, blood flow to that side of the brain is reduced and a stroke may result. In other cases, cholesterol particles from the atherosclerotic plaque may suddenly break off and enter the brain. In some people, these fragments come off from the heart and go to the brain. This often happens during a heart attack or an infection of the valves.[6]
Other reasons include excessive narrowing of large vessels resulting from an atherosclerotic plaque and increased blood viscosity caused by some blood diseases. TIA is related to other medical conditions such as hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.
TIA will usually be diagnosed after a doctor performs a history and a physical exam. There are several radiological tests that are done to evaluate patients who have had a TIA. This includes a CT scan or an MRI of the brain, ultrasound of the neck, an echocardiogram of the heart. In most cases, the source of atherosclerosis is usually identified with an ultrasound.[8]
Other diagnoses may have symptoms similar to those of a TIA:
A TIA may be prevented by changes in lifestyle; although most of these recommendations have no solid empirical data, most medical professionals believe them to be so. These include:
The mainstay of treatment following acute recovery from a TIA should be to diagnose and treat the underlying cause. It is not always immediately possible to tell the difference between a CVA (stroke) and a TIA. Most patients who are diagnosed at a hospital's emergency department as having suffered from a TIA will be discharged home and advised to contact their primary physician to organize further investigations. TIA can be considered as the last warning. The reason for the condition should be immediately examined by imaging of the brain.
The initial treatment is aspirin, second line is clopidogrel, third line is ticlopidine. If TIA is recurrent after aspirin treatment, the combination of aspirin and dipyridamole is needed (Aggrenox).
An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain. An echocardiogram is useful in detecting thrombus within the heart chambers. Such patients benefit from anticoagulation.
If the TIA affects an area supplied by the carotid arteries, an ultrasound (TCD) scan may demonstrate carotid stenosis. For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended. The blood vessel is opened up and the plaque is removed. The carotid may be replaced with a vessel retrieved from the lower leg or foot. The procedure is not technically difficult but carries the potential complication of inducing a stroke. A stroke can occur during surgery or after the procedure. The chance of a stroke ranges from 1–4 percent.[9]
Some patients may also be given modified-release dipyridamole or clopidogrel.
To reduce recurrence of an attack, ACE inhibitor drugs are used. The aim is to prevent a sudden, significant drop in blood pressure, because blood pressure that is too low may increase ischemic injury due to low perfusion.
The use of anti-coagulant medications, heparin and warfarin, or anti-platelet medications such as aspirin may be warranted. Antiplatelet drugs prevent platelets from sticking to each other, thus making the blood thinner (i.e., less viscous). Thinning the blood helps to ensure that small particles do not form and travel to the brain. These drugs require frequent monitoring. These drugs also have side effects such as easy bruising and bleeding from mild trauma.[10]
People diagnosed with a TIA are sometimes said to have had a warning for an approaching stroke. If the time period of blood supply impairment lasts more than a few minutes, the nerve cells of that area of the brain die and cause permanent neurologic deficit. One third of the people with TIA later have recurrent TIAs and one third have a stroke because of permanent nerve cell loss.
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